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Cancers, Volume 17, Issue 3 (February-1 2025) – 12 articles

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12 pages, 1827 KiB  
Article
Correlation Between Intravascular Platelet Aggregation in Tumors and Hypoxia-Inducible Factor 1 Alpha Expression in Epithelial Ovarian Cancer: Implications for Prognosis and Staging
by Jung Min Ryu, Yoon Young Jeong, Sun-Jae Lee and Youn Seok Choi
Cancers 2025, 17(3), 345; https://doi.org/10.3390/cancers17030345 (registering DOI) - 21 Jan 2025
Abstract
Background/Objectives: This study aimed to evaluate the association between intravascular platelet aggregation in tumors and ovarian carcinoma prognosis and investigate underlying mechanisms. Methods: A retrospective analysis was conducted on 144 patients with ovarian carcinoma. Immunohistochemical staining for CD42b, hypoxia-inducible factor-1α (HIF-1α), platelet-derived growth [...] Read more.
Background/Objectives: This study aimed to evaluate the association between intravascular platelet aggregation in tumors and ovarian carcinoma prognosis and investigate underlying mechanisms. Methods: A retrospective analysis was conducted on 144 patients with ovarian carcinoma. Immunohistochemical staining for CD42b, hypoxia-inducible factor-1α (HIF-1α), platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF) was performed using tissue microarrays to assess intravascular platelet aggregation. Staining grades ranged from 1 to 3 for CD42b (platelet aggregation or microthrombus) and 0 to 3 for HIF-1α, PDGF, and VEGF. Results: Among the patients, 25 (17.4%) had grade 1 (no platelet aggregation), 85 (59.0%) had grade 2 (platelet aggregation), and 34 (23.6%) had grade 3 (microthrombus). The grade of intravascular platelet aggregation in ovarian carcinoma was statistically significantly associated with a poor prognosis (p = 0.037). In addition, in patients with more advanced stages of ovarian cancer, higher levels of intravascular platelet aggregation were observed. Additional analysis revealed a correlation between platelet aggregation and HIF-1α expression (correlation coefficient = 0.226, p= 0.006), while PDGF and VEGF showed no significant correlations. Conclusions: Intravascular platelet aggregation in tumors is associated with advanced stages and poor prognosis in ovarian carcinoma. The results of our study suggest a potential association with hypoxia induced by intravascular platelet aggregation in ovarian carcinoma. Full article
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<p>Representative photos of intravascular platelet aggregation in tumors for each grade of CD42b immunohistochemical staining (×100). The staining was graded as follows: grade 1 (<b>A</b>), no intravascular platelet aggregation; grade 2 ((<b>B</b>), arrows), intravascular platelet aggregation in tumors; grade 3 ((<b>C</b>), arrowheads), intravascular microthrombus in tumors.</p>
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<p>Representative photos of each grade of hypoxia-inducible factor (HIF-1α), platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF) immunohistochemical staining (×200). The staining was graded as 0 if no malignant cells were stained, 1 if staining was weakly positive in &lt;1/3 of malignant cells, 2 if staining was weakly positive in &gt;2/3 of malignant cells or strongly positive in &gt;1/3 of malignant cells, and 3 if staining was weakly positive in most malignant cells or strongly positive in &gt;2/3 of malignant cells.</p>
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34 pages, 2998 KiB  
Article
An Assessment of Young Adults’ Awareness and Knowledge Related to the Human Papillomavirus (HPV), Oropharyngeal Cancer, and the HPV Vaccine
by Eric N. Davis and Philip C. Doyle
Cancers 2025, 17(3), 344; https://doi.org/10.3390/cancers17030344 (registering DOI) - 21 Jan 2025
Abstract
Background/Objectives: The human papillomavirus (HPV) is a prevalent sexually transmitted infection that is a known cause of morbidities such as genital warts and cancers of the cervix, anus, and oropharynx. Non-cervical HPV-related cancers have been a developing problem in North America, increasing in [...] Read more.
Background/Objectives: The human papillomavirus (HPV) is a prevalent sexually transmitted infection that is a known cause of morbidities such as genital warts and cancers of the cervix, anus, and oropharynx. Non-cervical HPV-related cancers have been a developing problem in North America, increasing in incidence by up to 225% in some instances over a span of two decades. Methods: This study investigated levels of awareness and knowledge of HPV, oropharyngeal cancer (OPC), and the HPV vaccine using a self-administered web-based survey designed specifically for this research. University students (n = 1005) aged 18–30 completed a 42-item questionnaire that included demographic information, awareness questions, and a series of “true/false/I don’t know” knowledge questions. Results: The data gathered revealed that participants had relatively high levels of awareness. However, many respondents had significant gaps in their knowledge of HPV, OPC, and the HPV vaccine. Collectively, the data indicate that awareness and knowledge of HPV and the value of vaccination may place younger individuals at risk for HPV-related infections. Conclusions: Although a relatively high level of awareness concerning HPV was observed, the gaps in knowledge suggest that further efforts are necessary to educate young adults. While all risk factors cannot be reduced, the present data may guide future efforts directed toward better education on HPV and related health concerns and associated risks. Full article
(This article belongs to the Special Issue Advances in Virus-Associated Head and Neck Cancer)
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<p>Age of participants. Note: 13 participants did not specify their age.</p>
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<p>Participant vaccination status.</p>
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<p>HPV knowledge sources.</p>
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<p>Perceived level of concern about HPV infection.</p>
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<p>Self-perceived HPV knowledge levels.</p>
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<p>Distribution of responses to HPV knowledge questions.</p>
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<p>Perceived level of concern about developing OPC.</p>
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<p>Self-perceived OPC knowledge levels.</p>
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<p>OPC knowledge questions and responses.</p>
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<p>HPV vaccine knowledge questions and responses.</p>
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13 pages, 619 KiB  
Article
Forty-Year Long-Term Outcome After Endoscopic and Open Surgery for Esthesioneuroblastoma in Consideration of Prognostic Factors
by Michael Koch, Matthias Balk, Sven Schlaffer, Abbas Agaimy, Heinrich Iro and Sarina K. Mueller
Cancers 2025, 17(3), 343; https://doi.org/10.3390/cancers17030343 (registering DOI) - 21 Jan 2025
Viewed by 45
Abstract
Background: The objective of this study was to compare results after endoscopic (ES) and open surgery (OpS) for esthesioneuroblastoma over a 40-year period. Methods: In a retrospective study, patients who had undergone ES and OpS for esthesioneuroblastoma with curative intent were included. The [...] Read more.
Background: The objective of this study was to compare results after endoscopic (ES) and open surgery (OpS) for esthesioneuroblastoma over a 40-year period. Methods: In a retrospective study, patients who had undergone ES and OpS for esthesioneuroblastoma with curative intent were included. The following outcome parameters were compared after ES and OpS: epidemiologic, clinical (including known tumor classifications), histopathologic, therapeutic (resection state, adjuvant therapy), and development of recurrences. Crude survival and Kaplan–Meier 10 y, 20 y, and 35 y actuarial survival were calculated. Results: Between 1981 and 2021, 15 patients were operated with ES and 28 with OpS. Advanced-stage tumors were significantly more often treated using OpS. For all other parameters, there were no other significant differences between ES and OpS. After ES, the 35 y OS, DSS, and DFS were 48.1%, 100%, and 55.9%, respectively. After OpS, they were 40.5%, 77.5%, and 35.3%. Conclusions: ES is an effective approach in esthesioneuroblastoma, even in the long-term course over decades, if the appropriate indication compared to OpS is respected. Full article
(This article belongs to the Section Clinical Research of Cancer)
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<p>10-, 20-, and 35-year DSS according to Kaplan–Meier after ES (1, blue color) and OpS (2, green color) of ENB (<span class="html-italic">p</span> = 0.071).</p>
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<p>10-, 20-, and 35-year DFS according to Kaplan–Meier after ES (1, blue color) and OpS (2, green color) of ENB (<span class="html-italic">p</span> = 0.402).</p>
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27 pages, 985 KiB  
Review
The Role of Macrophages in Various Types of Tumors and the Possibility of Their Use as Targets for Antitumor Therapy
by Enar Jumaniyazova, Anastasiya Lokhonina, Dzhuliia Dzhalilova, Ekaterina Miroshnichenko, Anna Kosyreva and Timur Fatkhudinov
Cancers 2025, 17(3), 342; https://doi.org/10.3390/cancers17030342 (registering DOI) - 21 Jan 2025
Viewed by 83
Abstract
In solid tumors, tumor-associated macrophages (TAMs) are one of the most numerous populations and play an important role in the processes of tumor cell invasion, metastasis, and angiogenesis. Therefore, TAMs are considered promising diagnostic and prognostic biomarkers of tumors, and many attempts have [...] Read more.
In solid tumors, tumor-associated macrophages (TAMs) are one of the most numerous populations and play an important role in the processes of tumor cell invasion, metastasis, and angiogenesis. Therefore, TAMs are considered promising diagnostic and prognostic biomarkers of tumors, and many attempts have been made to influence these cells as part of antitumor therapy. There are several key principles of action on ТАМs: the inhibition of monocyte/macrophage transition; the destruction of macrophages; the reprogramming of macrophage phenotypes (polarization of M2 macrophages to M1); the stimulation of phagocytic activity of macrophages and CAR-M therapy. Despite the large number of studies in this area, to date, there are no adequate approaches using antitumor therapy based on alterations in TAM functioning that would show high efficacy when administered in a mono-regimen for the treatment of malignant neoplasms. Studies devoted to the evaluation of the efficacy of drugs acting on TAMs are characterized by a small sample and the large heterogeneity of patient groups; in addition, in such studies, chemotherapy or immunotherapy is used, which significantly complicates the evaluation of the effectiveness of the agent acting on TAMs. In this review, we attempted to systematize the evidence on attempts to influence TAMs in malignancies such as lung cancer, breast cancer, colorectal cancer, cervical cancer, prostate cancer, gastric cancer, head and neck squamous cell cancer, and soft tissue sarcomas. Full article
(This article belongs to the Special Issue Macrophage-Directed Cancer Immunotherapy)
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<p>Types of tumor-associated macrophages.</p>
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16 pages, 1481 KiB  
Article
The ELECTRA Trial: Approach to Contemporary Challenges in the Development and Implementation of Double-Blinded, Randomised, Controlled Clinical Trials in Low-Volume High-Complexity Surgical Oncology
by Sean Ewings, Nadia Peppa, Daniel Griffiths, Maria Hawkins, Claire Birch, Adly Naga, Georgina Parsons, Aymen Al-Shamkhani, Joanne Lord, Adrian C. Bateman, Andrew Bateman, Charlotte Lane, Kelly Cozens, Gareth Griffiths, Simon J. Crabb, Charles West, Hideaki Yano, Malcolm A. West and Alexander H. Mirnezami
Cancers 2025, 17(3), 341; https://doi.org/10.3390/cancers17030341 - 21 Jan 2025
Viewed by 58
Abstract
Background: Achieving evidence-based practice change in surgery has always been challenging, with many aspects of common clinical practice evolving through lower-level studies that are susceptible to bias and confounding rather than high-quality evidence. This challenge is even more pronounced in the setting [...] Read more.
Background: Achieving evidence-based practice change in surgery has always been challenging, with many aspects of common clinical practice evolving through lower-level studies that are susceptible to bias and confounding rather than high-quality evidence. This challenge is even more pronounced in the setting of low-volume, high-complexity surgical oncology. Additionally, when the costs of interventions or technologies are high, designing and developing such studies within financially constrained national healthcare systems becomes even more complicated, potentially widening perceived healthcare inequalities between private and publicly funded systems. However, this is precisely the area where a lack of evidence can either hinder the development of significant new clinical advances or lead to the adoption of expensive and ineffective treatments. Here, we describe the novel approaches adopted in the design, development, and implementation of the ELECTRA trial, a randomised, controlled, double-blinded feasibility study with a planned extension to a late-phase trial. Methods: The Cancer Research UK ELECTRA (NCT05877352) trial is a three-armed randomised, controlled clinical trial designed to evaluate the incremental benefit of adding intraoperative electron beam radiotherapy (IOERT) to pelvic exenteration surgery for locally advanced and locally recurrent rectal cancer. ELECTRA is double-blinded, with patients, surgeons, and oncologists unaware of whether IOERT is administered or not. The primary feasibility outcome focuses on the ability to successfully recruit and randomise participants, while the subsequent primary outcome assesses IOERT field local control. Results: We describe the collaborative process involved in developing the trial, including national and international consultations to determine the best study design and the most optimal outcome measures to evaluate. We outline the extensive patient participation and input into the study design. Given the complexity and evolving nature of the field, with no clear international standardisations, we outline the processes used to address internationally agreed definitions, radiological standardisation, surgical learning curves, quality assurance, and pathological standardisation, as well as the broader impact and benefits of these activities. Finally, we describe the novel design utilised to facilitate the involvement of national and international units with varying levels of equipoise regarding IOERT. Conclusions: Historically, randomised clinical trials have not been the standard approach for evaluating surgical interventions due to their practical and methodological challenges, particularly in high-complexity, low-volume settings. Despite these difficulties, they remain the gold standard for evidence-based practice. The ELECTRA trial exemplifies a complex, innovative trial design that addresses an unmet need in a specialised area of high-complexity surgery. Using ELECTRA as an example, we highlight the genuine challenges in designing such complex trials and provide recommendations to facilitate the conduct of future well-designed surgical studies. Full article
(This article belongs to the Section Cancer Therapy)
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<p>Electra trial schema. SoC, Standard of care; sMDT, Specialist Multi-disciplinary Team.</p>
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<p>(<b>A</b>) View of the pelvic sidewall following pelvic exenteration and resection of pelvic sidewall including internal iliac vessels. The arrowheads show the application of metallic clips to the IOERT field for future tracking. (<b>B</b>) Similar view following pelvic exenteration with en bloc resection of the pelvic sidewall vessels exposing the sciatic nerve. The arrowheads and schematic oval shape show the site of the IOERT field. (<b>C</b>) Preoperative MRI of patient needing pelvic exenteration who was potentially eligible for the ELECTRA trial. The red circle shows the area at greatest risk of an R1 surgical resection. (<b>D</b>) Same patient in (<b>C</b>) postoperatively who received IOERT. The arrowheads show the ability to track the IOERT field with diagrammatic representation of the IOERT applicator as it would have been placed per-operatively.</p>
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36 pages, 1941 KiB  
Review
Current Landscape of Molecular Biomarkers in Gastroesophageal Tumors and Potential Strategies for Co-Expression Patterns
by Martin Korpan, Hannah Christina Puhr, Julia M. Berger, Alexander Friedrich, Gerald W. Prager, Matthias Preusser and Aysegül Ilhan-Mutlu
Cancers 2025, 17(3), 340; https://doi.org/10.3390/cancers17030340 - 21 Jan 2025
Viewed by 166
Abstract
The treatment of metastasized gastroesophageal adenocarcinoma largely depends on molecular profiling based on immunohistochemical procedures. Therefore, the examination of HER2, PD-L1, and dMMR/MSI is recommended by the majority of clinical practice guidelines, as positive expression leads to different treatment approaches. Data from large [...] Read more.
The treatment of metastasized gastroesophageal adenocarcinoma largely depends on molecular profiling based on immunohistochemical procedures. Therefore, the examination of HER2, PD-L1, and dMMR/MSI is recommended by the majority of clinical practice guidelines, as positive expression leads to different treatment approaches. Data from large phase-III trials and consequent approvals in various countries enable physicians to offer their patients several therapy options including immunotherapy, targeted therapy, or both combined with chemotherapy. The introduction of novel therapeutic targets such as CLDN18.2 leads to a more complex decision-making process as a significant number of patients show positive results for the co-expression of other biomarkers besides CLDN18.2. The aim of this review is to summarize the current biomarker landscape of patients with metastatic gastroesophageal tumors, its direct clinical impact on daily decision-making, and to evaluate current findings on biomarker co-expression. Furthermore, possible treatment strategies with multiple biomarker expression are discussed. Full article
(This article belongs to the Special Issue Oesogastric Cancer: Treatment and Management)
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<p>Comparison of the TAP to TPS and CPS. The visual estimation of tumor area positivity is less time consuming than counting each cell. CPS = combined positive score; IC = immune cell; <span class="html-italic">n</span>, number; PD-L1 = programmed death-ligand 1; TAP = tumor area positivity; TC = tumor cell; TPS = tumor proportion score.</p>
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<p>During the process of carcinogenesis, the loss of cellular polarity leads to aberrant Claudin 18.2 expression, which is associated with irregular proliferation and invasion.</p>
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13 pages, 2094 KiB  
Article
Downregulation of Aging-Associated Gene SUCLG1 Marks the Aggressiveness of Liver Disease
by Desislava K. Tsoneva, Alessandro Napoli, Mariya Teneva, Tommaso Mazza and Manlio Vinciguerra
Cancers 2025, 17(3), 339; https://doi.org/10.3390/cancers17030339 - 21 Jan 2025
Viewed by 197
Abstract
Introduction: The most common liver disease is nonalcoholic fatty liver disease, characterized by an intrahepatic accumulation of lipids that most often accompanies obesity. Fatty liver can evolve, in the presence of oxidative stress and inflammation, into disabling and deadly liver diseases such as [...] Read more.
Introduction: The most common liver disease is nonalcoholic fatty liver disease, characterized by an intrahepatic accumulation of lipids that most often accompanies obesity. Fatty liver can evolve, in the presence of oxidative stress and inflammation, into disabling and deadly liver diseases such as cirrhosis, hepatocellular carcinoma (HCC), and cholangiocarcinoma (CC). Old age seems to favor HCC and CC, in agreement with the inflammaging theory, according to which aging accrues inflammation. Cancer, in general, is an age-related disease, as incidence and mortality for most types of cancer increase with age. However, how molecular drivers in tumors differ or are mutated more frequently among patients of different ages remains scarcely investigated. A recent integrative analysis of the age-associated multi-omic landscape across cancers and healthy tissues demonstrated that age-related gene expression changes are linked to numerous biological processes. HCC and CC have among the lowest five-year survival estimates due to their aggressive progression. Materials and methods: In this study, we extracted top gene candidates from the above-mentioned pan-analyses (i.e., B2M, C1qA, SUCLG1) and tested by qPCR their expression and their correlation with disease progression in 48 tissue samples covering liver disease stages (fatty liver, hepatitis, cirrhosis, HCC and CC) and normal tissues. Results: Here, we report a significant downregulation in the expression of the age-associated gene SUCLG1 during the progression of liver disease toward HCC and CC, which also associates with poor patient survival. Conclusion: SUCGL1, a mitochondrial enzyme gene that catalyzes the conversion of succinyl CoA to succinate, might be therapeutically targeted for the development and progression of age-associated liver cancers with low survival rates. Full article
(This article belongs to the Special Issue Aging and Cancers)
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<p>SUCLG1 mRNA levels decrease with liver-tissue deterioration alterations. Expression mRNA levels of B2M, C1qA, and SUCLG1 in tissues with normal appearance (<span class="html-italic">n</span> = 9) or tissue specimen with diagnosis: Fatty liver (<span class="html-italic">n</span> = 5), hepatitis (<span class="html-italic">n</span> = 3), cirrhosis (<span class="html-italic">n</span> = 5), hepatocellular carcinoma (<span class="html-italic">n</span> = 24) or cholangiocarcinoma (<span class="html-italic">n</span> = 3). Significant differences are indicated by asterisks: &lt;0.05 (*), &lt;0.01 (**), and &lt;0.001 (***). All tissue samples in the liver cancer cohorts are biopsied from the tumor tissue area.</p>
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<p>Boxplot of SUCLG1 expression levels in tumor and control samples. The plot compares SUCLG1 expression levels (FPKM) in hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC) tumor samples with their respective normal control tissues. The analysis included 377 HCC tumor samples, 59 control HCC samples, 36 CC tumor samples, and 9 control CC samples. HCC tumor samples exhibit a median SUCLG1 expression of 10.69 FPKM, while the corresponding controls show a higher median expression of 11.76 FPKM. Similarly, CC tumor samples have a median SUCLG1 expression of 11.91 FPKM compared to a median of 11.56 FPKM in controls.</p>
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<p>Kaplan–Meier survival curves for SUCLG1 expression in HCC. Kaplan–Meier survival plots display the survival probabilities for patients grouped by SUCLG1 expression levels in hepatocellular carcinoma (HCC). In HCC, high SUCLG1 expression (≥12.58) was associated with improved survival compared to low expression (&lt;12.58) (log-rank test: <span class="html-italic">p</span> = 0.0419, χ2 = 4.14). The high-expression group comprised 24 samples, while the low-expression group included 330 samples.</p>
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<p>Kaplan–Meier survival curves for SUCLG1 expression in CC. Kaplan–Meier survival plots display the survival probabilities for patients grouped by SUCLG1 expression levels in cholangiocarcinoma (CC). In CC, patients with high SUCLG1 expression (≥10.39) had significantly better survival compared to those with low expression (&lt;10.39) (log-rank test: <span class="html-italic">p</span> = 0.0123, χ2 = 6.26). The high-expression group included 23 samples, while the low-expression group consisted of 13 samples.</p>
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17 pages, 1150 KiB  
Article
Parental Psychological Adjustment in Pediatric Acute Lymphoblastic Leukemia: The Mediating Role of Family Functioning and Resilience
by Ana Ferraz, Susana Faria, Mónica Jerónimo and M. Graça Pereira
Cancers 2025, 17(3), 338; https://doi.org/10.3390/cancers17030338 - 21 Jan 2025
Viewed by 120
Abstract
Background/Objectives: Acute lymphoblastic leukemia (ALL) is the most common pediatric cancer, with intense treatments affecting both children and their families. Limited information is available on parental distress and psychological well-being during the first treatment year, with most studies focusing on individuals rather than [...] Read more.
Background/Objectives: Acute lymphoblastic leukemia (ALL) is the most common pediatric cancer, with intense treatments affecting both children and their families. Limited information is available on parental distress and psychological well-being during the first treatment year, with most studies focusing on individuals rather than the family system. This study explores longitudinal changes in parental distress (psychological morbidity and traumatic stress symptoms), coping strategies, family resilience and functioning, and psychological well-being. The study also examines the mediating roles of family resilience, family functioning, and coping strategies in the relationships between parental distress and psychological well-being. Methods: A prospective study was conducted with 46 parents of children newly diagnosed with ALL, assessing parental distress, family functioning and resilience, coping, and psychological well-being across three treatment phases: consolidation (T0), delayed intensification (T1), and maintenance (T2). Results: Parental distress and family resilience significantly decreased from T0 to T2, while parental coping improved over time. Family functioning deteriorated from T0 to T1, stabilizing thereafter. Psychological well-being followed a non-linear trajectory, initially declining from T0 to T1 and improving from T1 to T2. Mediation analyses revealed that family resilience and family functioning partially mediated the relationships between parental distress and psychological well-being. Parental coping did not emerge as a mediator. Conclusions: Parental psychological adjustment in the context of ALL is dynamic and influenced by individual and family factors. Interventions that strengthen family functioning and resilience are crucial for supporting parental psychological well-being during treatment. A family-centered approach in healthcare delivery is essential to address individual and systemic challenges. Full article
(This article belongs to the Special Issue Novel Therapeutic Targets and Management in Pediatric Cancer)
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<p>Schematic overview and chronological timeline of the study.</p>
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<p>Schematic overview and chronological timeline of the study.</p>
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21 pages, 1714 KiB  
Review
The Role of Osteoprotegerin in Breast Cancer: Genetic Variations, Tumorigenic Pathways, and Therapeutic Potential
by Janan Husain Radhi, Ahmed Mohsen Abbas El-Hagrasy, Sayed Husain Almosawi, Abdullatif Alhashel and Alexandra E. Butler
Cancers 2025, 17(3), 337; https://doi.org/10.3390/cancers17030337 - 21 Jan 2025
Viewed by 187
Abstract
Introduction: Osteoprotegerin (OPG), encoded by the TNFRSF11B gene, is linked to the development of breast cancer via several pathways, including interactions with the receptor activator of nuclear factor-κB (RANK) ligands, apoptosis-inducing proteins like TRAIL, and genetic variations such as single nucleotide polymorphisms (SNPs), [...] Read more.
Introduction: Osteoprotegerin (OPG), encoded by the TNFRSF11B gene, is linked to the development of breast cancer via several pathways, including interactions with the receptor activator of nuclear factor-κB (RANK) ligands, apoptosis-inducing proteins like TRAIL, and genetic variations such as single nucleotide polymorphisms (SNPs), directly altering gene expression. This review aims to investigate the role of OPG expression in breast cancer. Methods: A comprehensive literature search was conducted using PubMed Medline, Google Scholar, and ScienceDirect. Only full-text English publications from inception to September 2024 were included. Results: Studies have demonstrated that certain SNPs in the OPG gene, specifically rs3102735 and rs2073618, are linked to a higher risk of breast cancer development. Additionally, OPG’s function as a TRAIL decoy receptor may inhibit the death of cancer cells. Furthermore, OPG in the serum and its interactions with BRCA mutations are being investigated for their potential influence on breast cancer progression. Studies have found that OPG promotes tumorigenesis by enhancing cell proliferation, angiogenesis, and aneuploidy in normal mammary epithelial cells. Moreover, OPG mediates the tumor-promoting effects of interleukin-1 beta and may serve as a biomarker for breast cancer risk, particularly in BRCA1 mutation carriers, through its role in dysregulated RANK signaling. Lastly, the use of recombinant OPG in mouse models has been found to exert anti-tumor effects. Conclusions: In this review, the role of OPG in breast cancer is examined. OPG has a multifaceted role in breast cancer tumorigenesis and exerts its effects through genetic variations (SNPs), interactions with TNF-related apoptosis-inducing ligand (TRAIL), and the modulation of the pro-tumorigenic microenvironment effects of angiogenesis, cell survival, and metastasis. Additionally, OPG’s dual role as a tumor suppressor and promoter serves as a possible therapeutic target to enhance apoptosis, limit bone metastasis, and modulate the tumor microenvironment. Whilst much is now known, further studies are necessary to fully delineate the role of OPG. Full article
(This article belongs to the Section Cancer Pathophysiology)
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<p>Osteoprotegerin (OPG) structure. OPG contains amino-terminal signal peptides and cysteine-rich tumor necrosis factor receptor (TNFR)-like domains, which are the key binding forces to the receptor activator of nuclear factor-κB (RANK). Additionally, OPG includes two death domain homologous regions of which the functions are currently not understood. A heparin binding domain limits the half-life of this molecule and serves as a basis for dimer formation [<a href="#B5-cancers-17-00337" class="html-bibr">5</a>].</p>
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<p>The OPG/RANK/RANKL pathway. A schematic to illustrate the OPG/RANK/RANKL pathway, which regulates bone remodeling by balancing osteoclast activation. The receptor activator of nuclear factor-κB ligand (RANKL) binds to the receptor activator of nuclear factor-κB (RANK) on osteoclast precursors, initiating a signaling cascade (via TRAF6 and NF-κB) that promotes bone resorption and is also involved in cellular proliferation. Osteoprotegerin (OPG) acts as a decoy receptor, binding RANKL to inhibit its interaction with RANK and prevent excessive osteoclast activity. Dysregulation of this pathway contributes to tumorigenesis. On the left, OPG binds to TNF-related apoptosis-inducing ligand (TRAIL), preventing its interaction with death receptors (DR4 and DR5) on tumor cells. This neutralization inhibits TRAIL-induced apoptosis, allowing cancer cells to survive.</p>
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<p>Osteoprotegerin (OPG)-mediated mechanisms in cancer progression. OPG enhances proliferation and promotes aneuploidy by activating chromosomal instability pathways involving Aurora A, Bub1, and BubR1 kinases, resulting in genomic disruption. Moreover, OPG drives neoangiogenesis by enhancing endothelial cell survival and vascular network formation through paracrine signaling, and facilitating tumor growth and progression, which is further reinforced by OPG’s ability to stimulate endothelial cell survival and differentiation. Moreover, OPG serves as a decoy receptor for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which prevents apoptosis. OPG also mediates protease activity, including cathepsin D and matrix metalloproteinase-2 (MMP-2), to facilitate cancer invasion and metastasis. Furthermore, single nucleotide polymorphisms (SNPs) associated with OPG (e.g., <span class="html-italic">rs3102735, rs2073617, rs2073618, rs4845627</span>) may influence susceptibility to malignancy.</p>
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<p>The role of osteoprotegerin (OPG) in inducing aneuploidy in mammary epithelial cells. A schematic to portray how osteoprotegerin (OPG) leads to chromosomal instability in human mammary epithelial cells (HMECs). The left panel represents a typical HMEC with a diploid genome and stable chromosomes. The middle panel shows the changes in the chromosomal integrity after the secretion of OPG in the tumor microenvironment. OPG has been shown to upregulate aneuploidy-related kinases such as Aurora A kinase (IAK-1), Bub1 kinase, and BubR1 protein, which disrupt mitotic checkpoint integrity and genomic stability. These regulatory effects underscore OPG’s contribution to driving aneuploidy and tumorigenesis. The right panel illustrates an aneuploid HMEC with disorganized chromosomes, highlighting the role of OPG in promoting chromosomal instability and aneuploidy, a key feature in cancer progression.</p>
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14 pages, 1325 KiB  
Systematic Review
Predicting Response to Treatment and Survival in Advanced Ovarian Cancer Using Machine Learning and Radiomics: A Systematic Review
by Sabrina Piedimonte, Mariam Mohamed, Gabriela Rosa, Brigit Gerstl and Danielle Vicus
Cancers 2025, 17(3), 336; https://doi.org/10.3390/cancers17030336 - 21 Jan 2025
Viewed by 157
Abstract
Background and Objective: Machine learning and radiomics (ML/RM) are gaining interest in ovarian cancer (OC) but only a few studies have used these methods to predict treatment response. The objective of this study was to review the literature on the applications of ML/RM [...] Read more.
Background and Objective: Machine learning and radiomics (ML/RM) are gaining interest in ovarian cancer (OC) but only a few studies have used these methods to predict treatment response. The objective of this study was to review the literature on the applications of ML/RM in OC assessments, specifically focusing on studies describing algorithms to predict treatment response and survival. Methods: This is a systematic review of the published literature from January 1985 to December 2023 on the use of ML/RM in OC An extensive search of electronic library databases was conducted. Two independent reviewers screened the articles initially by title then by full text. Quality was assessed using the MINORS criteria. p-values were generated using the Pearson’s Chi-squared (x2) test to compare the performances of ML/RM models with traditional statistics. Results: Of the 5576 screened articles, 225 studies were included. Between 2021 and 2023, 49 studies were published, highlighting the rapidly growing interest in ML/RM. Median-quality scores using the MINORS scale were similar between studies published between 1985–2021 and 2021–2023 (both 8). Neural Networks (22.6%) and LASSO (15.3%) were the most common ML/RM algorithms in OC. Among these studies, 13 focused specifically on prediction of treatment response using radiomics. A total of 5113 patients were analyzed. The most common algorithms were Random Forest (4/13) followed by Neural Networks (3/13) and Support Vectors (3/13). Radiomic analysis was used to predict response to neoadjuvant chemotherapy in seven studies, with a median AUC of 0.77 (range 0.72–0.93), while the median AUC was 0.82 (range 0.77–0.89) in the six studies assessing the prediction of optimal or complete cytoreduction. Median model accuracy reported in 7/13 studies was 73% (range 66–98%). Additionally, four studies investigated the use of ML/RM for survival prediction for OC. The XGBoost model had 80.9% accuracy in predicting 5-year survival compared to linear regression, which achieved 79% accuracy. The Random Forest model has 93.7% accuracy in predicting 12-month progression-free survival, compared to 82% for linear regression. Conclusions: In conclusion, we found that the use of ML/RM algorithms is becoming a more frequent method to predict responses to treatment of OC. These models should be validated in a prospective multicenter trial prior to integration into clinical use. Full article
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<p>PRISMA flow diagram of the study selection process.</p>
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<p>Common applications of machine learning in ovarian cancer among 224 studies.</p>
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<p>Pie chart of all ML techniques described in the included studies (<span class="html-italic">n</span> = 51) (others: UA&amp;MLR, CART, Elastic Net, naïve Bayes (NB), multi-layer perceptron (MLP), MLDTA, gradient-boosting machines (GBMs), MAC-Net, ELM, LDA, ResNet, Cox regression, SGD, DSS, MVA, K-mean clustering, and SE-SPP-DenseNet).</p>
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12 pages, 1306 KiB  
Article
Comprehensive Molecular Profiling of Metastatic Pancreatic Adenocarcinomas
by Vijay Antony, Tong Sun, Darin Dolezal and Guoping Cai
Cancers 2025, 17(3), 335; https://doi.org/10.3390/cancers17030335 - 21 Jan 2025
Viewed by 167
Abstract
Background: Pancreatic ductal adenocarcinoma (PDAC) is often diagnosed late, with an extremely poor prognosis. Treatment options like surgery, radiation, and chemotherapy are rarely curative. Tumor progression from primary to metastatic PDAC remains poorly understood at the molecular level. Methods: In the current study, [...] Read more.
Background: Pancreatic ductal adenocarcinoma (PDAC) is often diagnosed late, with an extremely poor prognosis. Treatment options like surgery, radiation, and chemotherapy are rarely curative. Tumor progression from primary to metastatic PDAC remains poorly understood at the molecular level. Methods: In the current study, we analyzed the molecular profiles of metastatic PDAC obtained via the Oncomine Comprehensive Assay in comparison to primary PDAC. Results: The current study cohort consisted of 115 metastatic PDAC cases, of which 71 (62%) cases succeeded in molecular testing while the remaining 44 (38%) cases contained insufficient tumor cells. Molecular profiling of 71 cases revealed a total of 239 molecular alterations, 3.4 alterations per case on average, predominantly in the form of gene mutations. The most common gene mutations included KRAS (86%) and TP53 (83%) mutations. Gene copy number alterations were also detected in 19 (27%) cases involving genes such as CCNE1 and ERBB2. Compared to the molecular profiles of primary PDAC reported in our prior study and TCGA database, there seemed to be increased rates of TP53, ARID1A, BRAF, and PIK3CA mutations in the metastatic diseases. Conclusions: These findings suggest that metastatic PDAC possesses unique genetic characteristics, offering potential therapeutic targets in advanced-stage pancreatic cancer. Full article
(This article belongs to the Special Issue Histology and Pathology of Pancreatic Cancer)
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<p>Molecular alterations in metastatic pancreatic adenocarcinoma.</p>
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11 pages, 208 KiB  
Review
Narrative Review of Single-Port Surgery in Genitourinary Cancers
by Olamide Omidele, Yuval Elkun, Christopher Connors, Ahmed Eraky and Reza Mehrazin
Cancers 2025, 17(3), 334; https://doi.org/10.3390/cancers17030334 - 21 Jan 2025
Viewed by 169
Abstract
Background: The da Vinci single-port (SP) platform is emerging as the latest innovation in minimally invasive surgery and its utilization in treating urologic malignancies continues to expand. Methods: A search was conducted in PubMed, MEDLINE, and ScienceDirect. The final set includes 40 academic [...] Read more.
Background: The da Vinci single-port (SP) platform is emerging as the latest innovation in minimally invasive surgery and its utilization in treating urologic malignancies continues to expand. Methods: A search was conducted in PubMed, MEDLINE, and ScienceDirect. The final set includes 40 academic articles. Results: Research on single-port surgery for genitourinary cancer is still an emerging topic. We divided the topic into the following categories: radical prostatectomy, radical cystectomy, nephrectomy, and nephroureterectomy. Conclusions: The single-port platform provides urologists with another tool to tackle more complex surgical cases and pathologies with the added improvements of decreased length of stay and increased pain tolerance for patients. Full article
(This article belongs to the Special Issue New Insights into Robotic Surgery for Urologic Cancer)
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